ArticleClinical and experimental immunology2010
Deficiency in activation-induced cytidine deaminase promotes systemic autoimmunity in lpr mice on a C57BL/6 background.
Article in Clinical and experimental immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Distributed clonal deletion prevents autoimmune disease progression.Cell reports · 2026Article
- Distributed Clonal Deletion Prevents Autoimmune Disease Progression.bioRxiv : the preprint server for biology · 2026Article
- Genetic Risk Variants for Class Switching Recombination Defects in Ataxia-Telangiectasia Patients.Journal of clinical immunology · 2022Article
- Article
- Abrogated AID Function Prolongs Survival and Diminishes Renal Pathology in the BXSB Mouse Model of Systemic Lupus Erythematosus.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Activation-induced cytidine deaminase deficiency accelerates autoimmune diabetes in NOD mice.JCI insight · 2018Article
- Article
- Functions and Malfunctions of Mammalian DNA-Cytosine Deaminases.Chemical reviews · 2016Review
- Self-Antigen-Driven Thymic B Cell Class Switching Promotes T Cell Central Tolerance.Cell reports · 2016Article
- Effect of TACI signaling on humoral immunity and autoimmune diseases.Journal of immunology research · 2015Review
- Broadening the translational immunology landscape.Clinical and experimental immunology · 2012Article
- LINE-1 retroelements complexed and inhibited by activation induced cytidine deaminase.PloS one · 2012Article
- Activation-induced cytidine deaminase (AID) is required for B-cell tolerance in humans.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Activation-induced cytidine deaminase mediates central tolerance in B cells.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Activation-induced deaminase-deficient MRL/lpr mice secrete high levels of protective antibodies against lupus nephritis.Arthritis and rheumatism · 2011Article
- PD-1 and LAG-3 inhibitory co-receptors act synergistically to prevent autoimmunity in mice.The Journal of experimental medicine · 2011Article
- Activation-induced cytidine deaminase and aberrant germinal center selection in the development of humoral autoimmunities.The American journal of pathology · 2011Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Activation-induced deaminase (AID) is a prerequisite for immunoglobulin (Ig) class-switch recombination and somatic hypermutation, which is critical for antibody affinity maturation. IgM and IgG autoantibodies are characteristic of the systemic autoimmune disorders such as lupus. However, the relative contributions of hypermutated high-affinity IgG antibodies and germline-encoded IgM antibodies to systemic autoimmunity are not defined fully. The role of AID in autoimmunity is unclear. The current study used AID-deficient mice to investigate the role of AID in the development and pathogenesis of murine lupus. C57BL/6 mice deficient in both Fas and AID were generated. Compared to their AID-competent littermates, AID(-/-) lymphoproliferative (lpr) mice produced significantly elevated levels of IgM autoreactive antibodies with enhanced germinal centre (GC) response, developed more advanced splenomegaly and exhibited more severe glomerulonephritis. Thus, AID may play an important role in the negative regulation of systemic autoimmune manifestations in murine lupus. The results also indicate that hypermutated high-affinity IgG antibodies are not necessary for the development of autoimmune syndrome in lpr mice on a C57BL/6 background.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.